Hemodialysis Vascular Access Dysfunction - InTech

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370 Progress in Hemodialysis – From Emergent Biotechnology to Clinical Practice of recent studies in AVGs have supported the concept of a migration of adventitial cells into the intima where they contribute to final neointimal volume 59,112. In addition, recent data from several experimental AVF stenosis models have shown that smooth muscle cells in the neointima, may in part, originate from bone-marrow-derived cells that bind to the site of vascular injury and later differentiate into a smooth muscle cell phenotype in the neointima 82,113,114. From a therapeutic standpoint, it is likely that better information about the true source of neointimal cells will allow for the development of novel therapeutic interventions targeting specific cell types. 3.3 Hemodynamic and vascular remodeling in hemodialysis access dysfunction A number of experimental studies have shown that turbulent, low flow, low fluid sheer stress are involved in neointimal hyperplasia development 115-119. High sheer stress has been associated with vascular dilatation through inhibition of smooth muscle cell proliferation and high levels of nitric oxide release, whereas low sheer stress has been associated with smooth muscle cell proliferation and lack of vasodilatation 120-123. Poor hemodynamic profiles could be a risk factor for neointimal hyperplasia development and poor venous dilatation, and the degree of luminal stenosis is dependent upon both the magnitude of neointimal hyperplasia and the capacity for vasodilatation or vasocontriction. Therefore, a significant amount of neointimal hyperplasia and medial hypertrophy may not result in luminal stenosis in the presence of adequate vasodilatation, while a small amount of neointimal hyperplasia, but with poor vasodilatation, may result in severe venous stenosis 4,124. Unfortunately, the factors that are responsible for vascular remodeling are unknown, but adventitial angiogenesis and scar formation are hypothesized to play a significant role 125,126. Thus, the ideal therapy for vascular stenosis would be an intervention that would prevent vascular constriction (adverse remodeling) and neointimal hyperplasia 4 4. Central venous dialysis catheters CVC dysfunction and related-infection remains a common cause of morbidity, mortality, and high economic costs in treating chronic hemodialysis patients. This section will provide a brief overview of catheter dysfunction and catheter-related infections. 4.1 Catheter dysfunction Catheter dysfunction can occur immediately after placement or in a catheter which has been previously functioning without difficulties, and most commonly manifests with low catheter blood flows during dialysis or negative arterial pressures on the dialysis machine 6. In more severe cases catheter thrombosis is characterized by the inability to aspirate blood from the dialysis port 6. Catheter dysfunction which occurs immediately after placement is most likely due to placement problems 6. Installation of a thrombolytic agent for 30 to 60 minutes is a treatment for catheter dysfunction, followed by a second installation if necessary 6. Recently published studies have reported varied success rate when treating catheter dysfunction with thrombolytics, ranging anywhere between 60-95% 26,28,35,127,128. When thrombolytic therapy is unsuccessful in providing adequate blood flow and adequate dialysis, despite repeated installations, then catheter exchange needs to be performed. The current K/DOQI guidelines recommends treatment with thrombolytic agents in all catheters with a persistently low blood flow rate (
Hemodialysis Vascular Access Dysfunction The current standard of care to prevent catheter thrombosis is installation of an anticoagulant in both dialysis ports at the completion of each dialysis session. In the United States, heparin is most commonly used, while in Europe citrate is the more common anticoagulant 6. The studies to-date have shown similar efficacy when comparing citrate to heparin for prophylaxis of catheter thrombosis, but with fewer complications of systemic bleeding with citrate 129-132. A recent multicenter, randomized-controlled trial has reported that use of a thrombolytic, tissue plasminogen activator as a locking solution compared to heparin had reduced incidence of catheter dysfunction 34. 4.2 Catheter-related bacteremia Currently, a precise definition for diagnosis catheter-related bacteremia is lacking. More rigorous definitions require a positive blood culture obtained from the catheter and a peripheral vein with the quantitative colony count being at minimum four-fold higher from the catheter sample 133. However, recently, the Infectious Disease Society of America has recognized the challenges in obtaining peripheral blood cultures from hemodialysis patients (e.g. priority for preserving veins and difficult cannulations) and has considered a definition of “possible” catheter-related bacteremia as positive blood culture obtained from the catheter in a symptomatic patient 134. The two main pathways where organisms can gain entry into the blood stream to initiate catheter-related bacteremia are intraluminal and extraluminal 135. Organisms gain entrance through the bloodstream extraluminally through contact between the skin surface organisms and the external surface of the catheter at the time of catheter placement or following catheter placement before healing of the exit site or endothelialization of the subcutaneous tunnel 7. Subsequently, the organisms colonize or migrate through the intracutaneous exterior tract of the catheter to the tip, allowing for hematagenous dispersion of the organisms and leading to catheter-related bacteremia 7. Intraluminal-derived infections results from the transfer of organisms from hand contact with the catheter, leading to contamination of the internal catheter surfaces 7. Infection from the extraluminal pathway most commonly occurs immediately after catheter insertion, while infections from the intraluminal pathway occurs throughout the life of the catheter 7. Irrespective of the route of bacterial entry, the bacteria will either adhere to the CVC or become incorporated into a fibrin sheath. Adherence of the bacterial organisms to the CVC initiates a common pathway of biofilm production. A mature biofilm is a self-sustaining colony of microorganism, guarded by an exopolysaccharide matrix, that is stimulated and secreted by the organism and very difficult to eradicate 7,136-140. Catheter-related bacteremia can result in devastating complications such as endocarditis, osteomyelitis, thrombophlebitis, septic arthritis, spinal epidural abscess, and large atrial thrombi 30,31,141-149. The majority of isolated organisms from catheter-related bacteremia are gram-positive organisms (52-84%) with Staph Aureus responsible for the majority of these organisms 7,30,31,143,150,151. Gram-negative are isolated in 27-36% of episodes and fungal isolated are relatively uncommon (
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